In another study, researchers found that the levels of fasting blood glucose, glucose tolerance and IR were all improved in mice with hepatocyte-specific deletion of HIF-1α; furthermore, liver changes in IL-1β and TNF-α in both HIF-1α knockout and IH-exposed mice were observed, implying that HIF-1α participated in the process of liver fibrosis in NASH through hepatic inflammation (38). The gene discussed is HIF1A; the disease is metabolic dysfunction-associated steatohepatitis.